Fecha de publicación: -- Fuente: PubMed "apiculture" Mol Immunol. 2026 Nov 5;200:44-55. doi: 10.1016/j.molimm.2026.10.005. Online ahead of print.ABSTRACTExcessive molecular and cellular immune activation can drive marked systemic increases in inflammatory mediators, a process associated with high mortality in several pathological conditions. Although signs of such responses have been reported in patients after Africanized honeybee swarm attacks, the inflammatory syndrome induced by Apis mellifera venom (AmV) remains poorly understood. Here, we investigated AmV-induced inflammatory responses using a lepirudin-based ex vivo human whole-blood model exposed to venom amounts delivered per sting, combined with functional and immunochemical assays. AmV rapidly elicited a robust inflammatory response, detectable within 15 min after experimental envenomation and progressively amplified over time. This response was marked by profound complement dysregulation, as shown by altered complement pathway activity, increased FBa fragments and C1-C1INH complexes, and a sharp decrease in MASP1-C1INH complexes. Complement activation was further supported by striking elevations in the anaphylatoxins C3a, C4a, and C5a, together with assembly of the terminal complement complex sC5b-9. In parallel, venom exposure induced sustained production of LTB4 and PGE2, excessive TXA2 release, and increased levels of several chemokines, including CCL2, CXCL8, CXCL9, and CXCL10, with particularly prominent release of CCL5. Together, these findings show that envenomation following Africanized honeybee swarm attacks triggers a hyperinflammatory syndrome that may contribute to venom-induced organ dysfunction. Our results uncover key immunopathological aspects of this condition and support excessive immune activation as a potential target for improved clinical management.PMID:42987495 | DOI:10.1016/j.molimm.2026.10.005